APOB and familial hyperaldosteronism: The most recent results demonstrate the efficiency of this approach (Shakhtshneider E. et al., 2019; Shakhtshneider E. V. et al., 2019), which facilitated examination of 42 patients with clinically diagnosed definite FH, resulting in detection of 12 different mutations in LDLR in 17 probands and two cases with a p.Arg3527Gln mutation in APOB. Thus, mutations were identified in 45% of families, of which 40% had changes in LDLR and 4.8% in APOB. No mutations associated with FH were found in PCSK9. Similarly, no homozygotes or compound-heterozygotes for mutations in LDLRAP1 (ARH) were observed.